Visfatin对心肌细胞炎性因子ICAM-1，VCAM-1表达的影响
发布时间：2019-05-15 01:20
【摘要】：LPS和Visfatin对细胞损伤方面的研究虽然有很多报道,但是有关两者对心肌细胞炎症共同作用的报道很少,所以有必要进行更加深入的研究。[研究背景]：Visfatin是最近几年发现的由内脏脂肪分泌的脂肪因子,对细胞的炎性产生及发展有一定的促进作用。LPS是革兰氏阴性细菌细胞壁的主要成分,是内毒素的特异性抗原,能够引起机体的微循环障碍。本文主要是研究Visfatin在LPS诱导的心肌细胞炎症作用方面的机制。[实验原理]：心肌细胞在LPS炎性模型中加入Visfatin,细胞外刺激使得I-κB激酶复合体活化, I-κB磷酸化,使得以无活性形式存于细胞浆中的NF-κB和I-κB的复合体分离,NF-κB暴露核定位位点,游离的NF-κB迅速移位,进入到细胞核,与特异性KB序列结合,诱导相关基因转录,引起粘附因子ICAM-1和VCAM-1的表达,诱导了白细胞的聚集和粘附,导致了多种炎症因子的表达,从而产生心肌损伤。[实验方法]：MTT法检测了不同浓度下的LPS和Visfatin对心肌的损伤程度,确定实验浓度。利用RT-PCR检测了粘附因子的mRNA表达情况后,并用Western blot法检测了相应蛋白表达,最后通过Western blot法检测了NF-κB p65的入核及I-κB的磷酸化情况。[实验结果]：在LPS、Visfatin单独处理的心肌细胞中发现ICAM-1和VCAM-1的表达量对比对照组均有所增加,二者共同作用时发现粘附因子的表达量明显高于单独处理组,而这个过程是通过I-KB的活化导致NF-κB入核,最终引起了下游粘附因子的表达途径,从而引起了心肌细胞的损伤,活性下降。 结论：Visfatin对LPS诱导的原代心肌细胞炎性因子ICAM-1和VCAM-1的表达具有显著的促进作用,而这一过程是通过I-κB的磷酸化降解释放出NF-κB复合体,增加了NF-κB p65的入核,启动了下游的粘附因子mRNA和蛋白的表达。
[Abstract]:Although there are many reports on cell injury caused by LPS and Visfatin, there are few reports on the interaction between them on cardiomyocyte inflammation, so it is necessary to carry out more in-depth study. [background]: LPs is a fat factor secreted by visceral fat discovered in recent years, which can promote the inflammatory production and development of cells. LPs is the main component of Gram-negative bacteria cell wall. It is a specific antigen of lipopolysaccharide, which can cause microcirculatory disturbance of the body. The purpose of this study was to study the mechanism of Visfatin in cardiomyocyte inflammation induced by LPS. [principle]: the extracellular stimulation of Visfatin, into the LPS inflammatory model activated the I-kappa B kinase complex and the phosphorylation of I-kappa B, resulting in the separation of the complexes of NF- and I-魏 B, which were stored in the cytoplasm in the form of inactivity, and the extracellular stimulation of the cardiomyocytes resulted in the activation of the I-kappa B kinase complex and the phosphorylation of the I-kappa B complex in the cytoplasm. NF- kappa B exposed to nuclear localization sites, free NF- kappa B rapidly shifted into the nucleus, bound to the specific KB sequence, induced the transcription of related genes, resulting in the expression of adhesion factors ICAM-1 and VCAM-1. It induced the aggregation and adhesion of leukocytes and led to the expression of many inflammatory factors, resulting in myocardial injury. [method]: MTT method was used to detect the degree of myocardial injury induced by LPS and Visfatin at different concentrations, and the experimental concentration was determined. The mRNA expression of adhesion factor was detected by RT-PCR, and the corresponding protein expression was detected by Western blot method. Finally, the nucleation of NF- 魏 B p65 and the phosphorylation of I-魏 B were detected by Western blot method. [results]: the expression of ICAM-1 and VCAM-1 in cardiomyocytes treated with LPS,Visfatin alone was significantly higher than that in the control group, and the expression of adhesion factor was significantly higher than that in the control group. This process leads to the entry of NF- kappa B into the nucleus through the activation of I-KB, and finally leads to the expression of downstream adhesion factor, which leads to the injury of cardiomyocytes and the decrease of activity. Conclusion: Visfatin can significantly promote the expression of inflammatory factors ICAM-1 and VCAM-1 in primary cardiomyocytes induced by LPS, and this process releases the NF- kB complex through the phosphorylation and degradation of I-魏 B and increases the nucleation of NF- 魏 B p65. The expression of downstream adhesion factor mRNA and protein was initiated.
【学位授予单位】：东北师范大学
【学位级别】：硕士
【学位授予年份】：2011
【分类号】：R363
本文编号：2477203
[Abstract]:Although there are many reports on cell injury caused by LPS and Visfatin, there are few reports on the interaction between them on cardiomyocyte inflammation, so it is necessary to carry out more in-depth study. [background]: LPs is a fat factor secreted by visceral fat discovered in recent years, which can promote the inflammatory production and development of cells. LPs is the main component of Gram-negative bacteria cell wall. It is a specific antigen of lipopolysaccharide, which can cause microcirculatory disturbance of the body. The purpose of this study was to study the mechanism of Visfatin in cardiomyocyte inflammation induced by LPS. [principle]: the extracellular stimulation of Visfatin, into the LPS inflammatory model activated the I-kappa B kinase complex and the phosphorylation of I-kappa B, resulting in the separation of the complexes of NF- and I-魏 B, which were stored in the cytoplasm in the form of inactivity, and the extracellular stimulation of the cardiomyocytes resulted in the activation of the I-kappa B kinase complex and the phosphorylation of the I-kappa B complex in the cytoplasm. NF- kappa B exposed to nuclear localization sites, free NF- kappa B rapidly shifted into the nucleus, bound to the specific KB sequence, induced the transcription of related genes, resulting in the expression of adhesion factors ICAM-1 and VCAM-1. It induced the aggregation and adhesion of leukocytes and led to the expression of many inflammatory factors, resulting in myocardial injury. [method]: MTT method was used to detect the degree of myocardial injury induced by LPS and Visfatin at different concentrations, and the experimental concentration was determined. The mRNA expression of adhesion factor was detected by RT-PCR, and the corresponding protein expression was detected by Western blot method. Finally, the nucleation of NF- 魏 B p65 and the phosphorylation of I-魏 B were detected by Western blot method. [results]: the expression of ICAM-1 and VCAM-1 in cardiomyocytes treated with LPS,Visfatin alone was significantly higher than that in the control group, and the expression of adhesion factor was significantly higher than that in the control group. This process leads to the entry of NF- kappa B into the nucleus through the activation of I-KB, and finally leads to the expression of downstream adhesion factor, which leads to the injury of cardiomyocytes and the decrease of activity. Conclusion: Visfatin can significantly promote the expression of inflammatory factors ICAM-1 and VCAM-1 in primary cardiomyocytes induced by LPS, and this process releases the NF- kB complex through the phosphorylation and degradation of I-魏 B and increases the nucleation of NF- 魏 B p65. The expression of downstream adhesion factor mRNA and protein was initiated.
【学位授予单位】：东北师范大学
【学位级别】：硕士
【学位授予年份】：2011
【分类号】：R363
【参考文献】
相关期刊论文 前1条
1 郑炜,赵小燕;浅谈脂多糖对机体的影响[J];甘肃中医学院学报;1998年S1期
，本文编号：2477203
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